Biological Responses to Diesel Exhaust Particles (DEPs) Depend on the Physicochemical Properties of the DEPs

Abstract

Diesel exhaust particles (DEPs) are the main components of ambient particulate materials, including polyaromatic hydrocarbons (PAHs), n-PAHs, heavy metals, and gaseous materials. Many epidemiological, clinical, and toxicological studies have shown that ambient particles, including DEPs, are associated with respiratory disorders, such as asthma, allergic rhinitis, and lung cancer. However, the relationship between the biological response to DEPs and their chemical composition remains unclear. In this study, we investigated the physicochemical properties of DEPs before toxicological studies, and then administered a single intratracheal instillation of DEPs to mice. The mice were then killed 1, 7, 14 and 28 days after DEP exposure to observe the biological responses induced by DEPs over time. Our findings suggest that DEPs engulfed into cells induced a Th2-type inflammatory response followed by DNA damage, whereas DEPs not engulfed into cells induced a Th1-type inflammatory response. Further, the physicochemical properties, including surface charge, particle size, and chemical composition, of DEPs play a crucial role in determining the biological responses to DEPs. Consequently, we suggest that the biological response to DEPs depend on cell-particle interaction and the physicochemical properties of the particles.

Exposure to allergen and diesel exhaust particles potentiates secondary allergen-specific memory responses, promoting asthma susceptibility

“…In contrast to HDM, which is rapidly degraded, DEP or at least its carbon core persists within phagocytic cells for weeks 25 . We assessed how long DEP persisted in lungs following a single exposure of DEP and found numerous DEP positive cells in the lungs 3 months later.…”

Pilot Metabolome-Wide Association Study of Benzo(a)pyrene in Serum From Military Personnel

“…Exposure to diesel fuel particles has been shown to increase allergic inflammation in both animal models and humans through increased local antigen-specific immunoglobulin E and cytokine release (43-45). In addition, animal and in vitro models of BaP exposure have indicated increases in histamine production following exposure periods (46, 47). While histamine was deceased in our study, association with BaP level nonetheless suggests changes in metabolic pathways important to immune response.…”

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“…33,34 It has been proposed that when diesel-exhaust particles are engulfed by macrophages, a Th2-type inflammatory response is induced, whereas diesel-exhaust particles that are not engulfed produce a Th1-type inflammatory response. [35][36][37] High carbon dioxide concentrations in the environment increase both pollen production and the allergenicity of pollen. Indeed, Singer et al 38 showed that high concentrations of carbon dioxide enhanced the production of Amb a 1, an allergenic protein in ragweed pollen, while Ziska et al 39 reported that in urban locations where carbon dioxide concentrations are higher, ragweed produces greater amounts of pollen (which contains the Amb allergen) than it does in rural locations.…”